The main objective of this project is to determine the nature of the regulatory mechanisms controlling protein synthesis during normal development of the mouse central nervous system. Whether multiple species of the tissue-specific S-100 protein represent primary gene products or are the result of posttranslational modification will be determined. Experiments to examine the cause of an increase in glutamic acid decarboxylase activity during postnatal CNS development will be performed. Studies on mouse CNS mutants will also be carried out to ascertain if any of these involve quantitative or qualitative alterations in cellular proteins. BIBLIOGRAPHIC REFERENCE: Stewart, J.A., Contribution of a change in mRNA half-life to the accumulation of the tissue-specific S-100 protein during postnatal development of the mouse brain. Developmental Biology 44, 178-186, 1975.